Experimental pain modulation via hypnosis: Neurophysiological perspectives

This chapter reviews key electrophysiological and neuroimaging findings on the neural mechanisms underlying hypnosis and its modulation of experimentally induced pain, with an emphasis on the roles of hypnotizability and the content of suggestions. Highly hypnotizable (HH) individuals consistently report reduced pain and emotional distress under hypnotic hypoalgesia, although effects on somatosensory-evoked potentials (SERPs) vary due to methodological differences in induction techniques and experimental paradigms. EEG time-frequency analyses and oscillatory studies offer more consistent results, particularly in HH individuals, highlighting gamma-band oscillations as markers that distinguish hypnosis from distraction. Neuroimaging studies demonstrate that hypnotic hypoalgesia engages distributed brain networks, with activity changes in the anterior and medial cingulate cortices (ACC and MCC), thalamus, primary sensory cortex, dorsolateral prefrontal cortex, and insula correlating with the modulation of pain's sensory and affective dimensions. Functional connectivity analyses reveal enhanced interactions between the ACC, periaqueductal gray (PAG), and insula during preparatory suggestion phases relative to a control condition. Additionally, hypnosis influences autonomic nervous system function by reducing sympathetic arousal and enhancing parasympathetic tone. Overall, hypnosis emerges as a multifaceted process shaped by individual susceptibility, the induction method, and the structure of suggestions, engaging diverse neural pathways that support its potential as a personalized tool for pain management.